Shock

Management of Shock – Alex Toporex, Soibhan Kelley

Distributive Shock

Background

  • Pathophysiology: severe, peripheral vasodilation
    • CO/CI increased, SVR decreased, PCWP and RAP normal to low
  • Etiologies: sepsis (far and away the most common cause of distributive shock), anaphylaxis, neurogenic, adrenal insufficiency, pancreatitis
  • Signs/symptoms:
    • Sepsis: localizing signs of infection; tachycardic, tachypnic, may be hypo/hyperthermic; POCUS with hyperdynamic cardiac function
    • Anaphylaxis: history of anaphylaxis; urticaria, edema, diarrhea, wheezing on exam
    • Neurogenic: history of CNS trauma; focal neurologic deficits on exam
    • Adrenal insufficiency: hx chronic steroid use, may have GI symptoms, hyponatremia (common), hyperkalemia (rare), hypoglycemia, hypo/hyperthermia, NAGMA
    • Pancreatitis: abdominal pain, elevated lipase, evidence on CT scan

 

Management

  • Sepsis: see sepsis section
  • Anaphylaxis: 0.3mg IM epinephrine ASAP to be repeated q5-15min x 3; after third IM epi, consider IVF and epi gtt if persistent hypotension. Adjuncts: albuterol nebs for bronchospasm, H1 and H2 blockers (Benadryl 25-50mg IV, ranitidine 50mg IV), +/- glucocorticoids (methylprednisolone 1mg/kg). EPINEPHRINE SAVES LIVES.
  • Neurogenic: caution with IVF resuscitation, which can worsen cerebral and spinal cord edema; preferred pressors are norepinephrine and phenylephrine; for neurogenic shock 2/2 spinal cord pathology, consider higher MAP goal 85-90 mmHg
  • Adrenal insufficiency: initiate stress dose steroids with hydrocortisone 100mg IV q8hr or 50mg q6hr; can also trial stress dose steroids on pts on 2-3 pressors
  • Pancreatitis: IVF (though at risk for over-resuscitation) + pressors; trend H/H and Ca; treat complications (necrotizing pancreatitis, abdominal compartment syndrome); address underlying etiology (gallstones, hypertriglyceridemia, hypercalcemia)

 

Cardiogenic Shock

Background

  • Pathophysiology: CO/CI decreased, SVR increased, PCWP and RAP elevated (left heart failure) or PCWP low/normal and RAP elevated (right heart failure)
  • Etiologies: Cardiomyopathy (LHF, RHF or biventricular), Arrhythmia, Mechanical such as acute AR (ex: dissection) or MR (ex: ruptured papillary muscle)

 

Presentation

  • Edematous, elevated JVP, “cold and wet”; hypoxia w/crackles and pulm edema on CXR; mixed venous sat < 50-60%; POCUS with plump, non-compressible IVC, reduced EF, and B-lines

 

Management

Immediate assessment for acute ischemic event

  • Pulmonary artery catheters may be helpful for titrating therapies
  • Hallmark therapies:
        • Preload aggressive diuresis, frequently need bumex or lasix gtt
        • Inotropy dobutamine or milrinone gtt, both can cause arrhythmias, hypotension, reflex tachycardia; epi is also a good choice and a more familiar choice for MICU staff. Caution with milrinone in renal dysfunction.
        • Afterload Reduction nitroglycerine gtt; hydralazine + ISDN for PO options; treat hypotension with pressors/inotropes if needed
  • Acute Right Heart Failure is highly susceptible to R-sided coronary ischemia, consider vasopressin as beneficial in improving R-sided coronary blood flow
  • Arrhythmia: See mgmt in “arrhythmia,” In general, unstable tachyarrhythmia cardioversion. Unstable bradyarrhythmia pacing. Avoid negative inotropes (BB, CCB)

 

Hypovolemic Shock

Background

  • Etiologies: Hemorrhagic and non-hemorrhagic
  • Signs/symptoms:
    • Hemorrhagic: Common sources include GI, retroperitoneal (*needs high index of suspicion), traumatic. Other sources of significant hemorrhage include intraabdominal, thighs, thorax.
    • Non-hemorrhagic: generally 2/2 GI losses—history of diarrhea, emesis; can also be 2/2 decreased PO intake
    • POCUS with thin, collapsible IVC

 

Management (Hemorrhagic)

  • Ensure good access with two large-bore (at least 18G) IVs ideally in AC or above; Cordis or MAC CVC (can also use dialysis catheter, if necessary)
  • Hyperacute bleed:
    • 1:1:1 ratio FFP:Plt:RBC (balanced resuscitation), massive transfusion protocol (MTP)
    • Monitor iCa and replete (citrated blood products will deplete Ca)
    • Minimize crystalloid, if possible, w/primary use to prevent immediate hemodynamic collapse (contributes to coagulopathy, hypothermia, acidemia, trauma/surgery)
    • Permissive hypotension until source control/transfusions with arterial bleeds (high MAP/SBP --> clot destabilization); trend POC lactate/exam to guide
    • Acute traumatic arterial bleed or post-partum hemorrhage consider TXA (1-2 gm bolus)
    • Reverse anticoagulation, if applicable
    • Vasopressors --> generally poorly effective, would start with norepinephrine
    • Source control --> GI, IR, or EGS
  • Variceal bleed: See GI Bleeding section for specific management

 

Management (Non-Hemorrhagic)

  • Aggressive IVF resuscitation (balanced crystalloid); target MAP ≥65
  • Can support BP during resuscitation with pressors (usually norepinephrine)

 

Obstructive Shock

Background

  • Etiologies:
    • Massive pulmonary embolism, tension pneumothorax, and cardiac tamponade
  • Signs/symptoms:
    • Pulmonary embolism: acute hypotension, known DVT, evidence of R heart strain on EKG, POCUS w/enlarged RV, septal bowing, McConnell’s sign, BNP, PE on CTA
    • Tension pneumothorax: history of COPD or fibrotic lung disease, ventilated pts w/ high peak pressures, unilateral decreased BS on auscultation and tympany on percussion, POCUS without lung sliding, CXR w/ PTX and mediastinal shift
    • Cardiac tamponade: elevated JVP, muffled heart sounds, pulsus paradoxus, POCUS with diastolic collapse of RV and large pericardial effusion (best in subcostal window)

 

Management

  • Massive pulmonary embolism: see Pulmonary Embolism Section for specific management
  • Tension PTX: needle decompression using 14-16G needle into the second intercostal space at the midclavicular line; call thoracic surgery or fellow for chest tube ASAP
  • Cardiac tamponade: STAT page cardiology or cardiothoracic surgery; can temporize hypotension with IVF resuscitation—500-1L IVF boluses (may not work if pt is euvolemic or hypervolemic); no proven benefit from inotropy (e.g., dobutamine)